Knockdown of JMJD3 ameliorates cigarette smoke extract-triggered bronchial epithelial cell injury via ACSL4-dependent ferroptosis

Qin, Ruijun; Wang, Ping; Li, Lingzhi

doi:10.1016/j.tiv.2023.105731

Toxicology in Vitro

2024

DOI: 10.1016/j.tiv.2023.105731

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Knockdown of JMJD3 ameliorates cigarette smoke extract-triggered bronchial epithelial cell injury via ACSL4-dependent ferroptosis

Ruijun Qin,

Ping Wang,

Lingzhi Li

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Cited by 3 publications

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Acacetin Attenuates Cigarette Smoke Extract-Induced Human Bronchial Epithelial Cell Injury by Activating NRF2/SLC7A11/GPX4 Signaling to Inhibit Ferroptosis

Chen,

Wu,

Dong

et al. 2025

Cell Biochem Biophys

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Acacetin Attenuates Cigarette Smoke Extract-Induced Human Bronchial Epithelial Cell Injury by Activating NRF2/SLC7A11/GPX4 Signaling to Inhibit Ferroptosis

Chen,

Wu,

Dong

et al. 2025

Cell Biochem Biophys

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A comprehensive review of ferroptosis in environmental pollutants-induced chronic obstructive pulmonary disease

Jiang,

Peng,

et al. 2024

Science of The Total Environment

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Fluorofenidone alleviates cigarette smoke exposure-induced chronic lung injury by targeting ferroptosis

Wu,

Li,

Xuan

et al. 2024

Sci Rep

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Chronic obstructive pulmonary disease (COPD) is a common condition that poses significant health risks to humans. Pulmonary interstitial fibrosis (PIF) often manifests in advanced stages of COPD. Fluorofenidone (AKF) has a wide range of pharmacological effects, including anti-fibrotic, antioxidant, and anti-inflammatory effects. Therefore, this study aimed to assess the role of AKF in lung injury and its underlying mechanisms. The COPD mice model was constructed by cigarette smoke (CS) combined with lipopolysaccharide (LPS) treatment. The effect of AKF on COPD mice was evaluated by lung injury, lipid peroxidation, inflammatory factors, and the expression of ferroptosis markers. Furthermore, the normal human bronchial epithelial cell line, Beas-2B, was used to verify the mechanism underlying the association between ferroptosis and inflammation. AKF attenuated the cigarette smoke (CS)/LPS-induced inflammatory response in the mouse lungs. Additionally, AKF attenuated the CS/LPS-induced fibrosis response in the mouse lungs. AKF inhibits ferroptosis in lung tissues of CS/LPS-exposed mice. Furthermore, AKF suppressed the inflammatory response and ferroptosis in CSE-treated BEAS-2B cells via NF-κB signaling pathway. AKF can function as a novel ferroptosis inhibitor by inhibiting NF-κB to inhibit airway inflammation and fibrosis, providing a scientific basis for the use of AKF to prevent the progression of COPD and pulmonary fibrosis. Supplementary Information The online version contains supplementary material available at 10.1038/s41598-024-83998-w.

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Knockdown of JMJD3 ameliorates cigarette smoke extract-triggered bronchial epithelial cell injury via ACSL4-dependent ferroptosis

Cited by 3 publications

References 42 publications

Acacetin Attenuates Cigarette Smoke Extract-Induced Human Bronchial Epithelial Cell Injury by Activating NRF2/SLC7A11/GPX4 Signaling to Inhibit Ferroptosis

Acacetin Attenuates Cigarette Smoke Extract-Induced Human Bronchial Epithelial Cell Injury by Activating NRF2/SLC7A11/GPX4 Signaling to Inhibit Ferroptosis

A comprehensive review of ferroptosis in environmental pollutants-induced chronic obstructive pulmonary disease

Fluorofenidone alleviates cigarette smoke exposure-induced chronic lung injury by targeting ferroptosis

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